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Medische Microbiologie > Bacteriologie > Flashcards

Bacteriologie Flashcards

1
Q

Virulence factors S. aureus

A

Toxins: cytolytic, enterotoxins, exfoliative toxins
Enzymes: coagulase, hyaluronidaselipase, fibrinolysis, catalase

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2
Q

bad bacteria in microbiome

A

Neisseria meningitidis
streptococcus pneumoniae
s. aureus

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3
Q

virulence definition

A

degree of pathogenicity (ability to produce disease) of the microbe

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4
Q

virulence factors, examples

A

adhesins, invasins, capsule, toxins, enzymes, pili

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5
Q

gram+ bacteria divided into 2 subgroups

A

cocci

bacilli

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6
Q

what type of bacterium is N. meningitidis

A

gram negative diplococcus

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7
Q

what does bromelia burgdorferi cause?

A

lyme disease

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8
Q

wat is serologie?

A

het aantonen van immunoglobulinen tegen agens

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9
Q

welke vormen hebben deze soorten respectievelijk: coccus, baccillus, spirochetes

A

sphere, rod, spiral

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10
Q

what is MIC?

A

minimal inhibitory concentration –> sterkste verdunning waarbij bacterie niet meer groeit

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11
Q

voorbeelden moeilijk kwetsbare bacteriën

A

mycobacterium, mycoplasma, chlamydia, legionella

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12
Q

what kind of bacterium is N. meningitidis

A

gram negative diplococcus (meningococcus)

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13
Q

4 steps of invasive meningococcal disease (IMD):

A
  1. colonization
  2. invasion epithelium
  3. invasion blood (septicaemia)
  4. dissemination (to CSF)
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14
Q

4 results meningococcemia (meningococci in bloodstream)

A
  1. sepsis
  2. rash
  3. disseminated intravascular coagulation (DIC); abnormal blood clotting
  4. meningitis
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15
Q

what determines meningococcal serogroup, and how many are there?

A

polysaccharide capsule

13

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16
Q

2 typing methods for N. meningitidis

A

phenotype and genotype

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17
Q

annotation for N. meningitidis

A

Example: Nm: B:P1.7,4:F5-1

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18
Q

what methods can be used in genotype typing for N. meningitidis, and what do they do?

A
  1. multi locus sequence typing (MLST), sequencing of 7 loci
  2. ribosomal MLST, sequencing of 53 loci

these methods assign numbers to alleles

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19
Q

what does the sequence type (ST) of N. meningitidis say?

A

the combination of allele numbers, assigned by MLST

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20
Q

what is a singleton?

A

a strain that doesn’t belong to a certain clonal complex (CC, a complex matching the central genotype)

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21
Q

what clonal complexes (CC) overrepresented in patients with IMD

A

CC41/44 & CC32

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22
Q

What clonal complexes are overrepresented in carriers

A

CC53 & CC35 (no capsules, important virulence factor)

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23
Q

why is there no MenB vaccine?

A

CPS of B is poorly immunogenic; it is identical to sialic acid in nerve tissue

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24
Q

what does Factor H binding protein (FHbp) do?

A

enables microbe to bind factor H (from complement) enabling bacterial survival in blood

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25
Q

what is an important AMP and what does it do

A

Lactoferin; pulls away iron from pathogens

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26
Q

what is GAS

A

Group A Streptococcus (Streptococcus pyogenes)

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27
Q

what causes impetigo?

A

S. aureus: exfoliated toxin

GAS

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28
Q

major component of cell wall S. aureus

A

protein A

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29
Q

what does S. aureus toxin panton valentine do, and what kind of toxin is it?

A

destroys leukocytes, exotoxin

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30
Q

what kind of bacterium is S. pyogenes (GAS)

A

gram positive, from chain structures

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31
Q

exotoxins secreted by GAS

A

SPE: A, B and C

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32
Q

3 examples of invasins and adhesins from GAS

A

Invasins:

  1. streptolysins
  2. streptokinases
  3. proteases

adhesins:

  1. M protein (in fimbriae)
  2. lipoteichoic acid (LTA)
  3. protein F and Sfb
33
Q

what is a BAI?

A

biomaterial associated infection:
e.g. breast implants, CSF shunts, pacemaker

often caused by staph epidermis

34
Q

through which 3 mechanisms can staphylococci form biofilms

A
  1. through exopolysaccharide production
  2. through release of DNA
  3. through factors of proteic nature
35
Q

how does a s. aureus biofilm detach

A

via phenol soluble modulins (PSM)

36
Q

describe biofilm process

A
  1. biofilm formation (through 3 mechanisms)
  2. primary attachment phase (MSCRAMM & Aap)
  3. accumulation phase
  4. detachment (PSMs)
37
Q

rifampicine mechanism

A

inhibits RNA synthesis by inhibiting RNA pol

38
Q

tetracycline mechanism

A

inhibits protein synthesis by inhibiting ribosomes

39
Q

kanamycin mechanism

A

inhibits protein synthesis by binding to bacterial 30S ribosomal subunit, causing misreading of tRNA

40
Q

penicillin mechanism

A

inhibits cell wall synthesis by blocking peptidoglycan production

41
Q

3 virulence factors Proteus mirabilis

A
  1. urease
  2. flagella
  3. fimbriae
42
Q

what is a McConkey plate

A

selective plate for Gram neg bacteria

43
Q

difference S. aureus and proteus mirabilis?

A

s. aureus is non motile, p. mirabilis is motile

44
Q

what kind of bacterium is p. mirabilis

A

gram neg bacilli, with flagella to move

45
Q

true or false: more fimbriae = more bacteria colonizing

46
Q

3 point hierarchy of fimbriae regulatory mechanisms

A
  1. DNA structure
  2. transcriptional regulation
  3. post transcriptional regulation (sRNA)
47
Q

mrp fimbriae gene cluster expression in high and low oxygen

A

high oxygen: phase off; flagellum expression by not expressing mrpJ
low oxygen: phase on; flagellum inhibition by expressing mrpJ

48
Q

what does mrpJ do

A

block flhD/C, which code for flagella

49
Q

is chlamydia trachomatis gram neg or pos

50
Q

what kind of bacterium is neisseria gonorrhoea

A

gram neg diplococci

51
Q

what does Treponema palladium (a spirochete) cause

52
Q

which 2 bacteria in the family of Neisseriaceae are the only pathogens in this family

A

N. gonorrhoeae and N. meningitidis

53
Q

4 antibiotic resistance mechanisms is N. gonorrhoeae

A
  1. plasmid mediated
  2. mutations in antibiotic binding site
  3. mutations in topo-isomerase
  4. overexpression of efflux pumps
54
Q

how does N. gonorrhoeae acquire tetracyclin resistance

A

through tetM sequence on conjugative plasmid. It protects the ribosome from binding the antibiotic

55
Q

2 toxins attracting and killing neutrophils

A

S. aureus: PVL, PSM

56
Q

3 mechanisms of defense on neutrophils

A
  1. block of chemotaxis (CHIPS)
  2. toxins
  3. biofilm formation
57
Q

4 complement evasion mechanisms by microorganisms

A
  1. capsule prevents complement activation
  2. LPS prevents C3b contact
  3. LPS prevents C3 and MAC
  4. factor H binding molecules; degrading C3b
58
Q

5 mechanisms for antibody evasion

A
  1. phase variation
  2. antigenic variation
  3. decoy: capture/block antibody
  4. Ig-proteases
  5. Fc receptors
59
Q

how do salmonella, proteus and s. aureus evade AMPs?

A

salmonella: phoP/Q pmrA/B: inducible aminoarabinose
proteus: aminoarabinose on LPS
s. aureus: via dlt operon; D-alanine in LTA. and QacA exporters

60
Q

name 2 microorganisms that can cause endocarditis and if they can infect WITH or WITHOUT pre existing heart vegetation

A

s. aureus; without

viridans streptococcus; with

61
Q

4 s. aureus virulence factors in endocarditis

A
  1. capsule
  2. adhesins (FnBP, CflA, Protein A)
  3. toxins
  4. exoenzymes
62
Q

3 viridans streptococci virulence factors

A
  1. exopolysaccharides (glucans, fructans)
  2. MSCRAMM
  3. PAAP
63
Q

what are thrombocidins (TC) and what do they do

A
  • compound preventing endocarditis

- C terminally truncated derivatives of CXC chemokines

64
Q

what is a potential role for platelets in endocarditis

A

formation of vegetation; susceptible to endocarditis

65
Q

what do activated platelets secrete

A

Platelet Basic Protein (PBP)

66
Q

what results from N terminal truncations of PBP, and in turn C terminal truncation of these products?

A
  • CTAP-III and CXC-L7; fibroblast activation and neutrophil chemotaxis
  • C terminal truncation of these results in TC-1 and 2 –> highly potent AMPs
67
Q

which 2 receptors do platelets have for IgA and IgE and what do they induce

A
  • MHC-I and Fc

- activate complement

68
Q

what 4 antigens do TLR receptors on macrophages and monocytes bind

A
  1. LPS
  2. peptidoglycan
  3. LTA
  4. flagellin
69
Q

which 3 pathogens cause sinusitis

A
  1. S. pneumoniae
  2. Moraxella catharallis
  3. H. influenzae
70
Q

name virulence factors for GAS (6)

A

exotoxins (SPE A, B and C), M protein, LTA, capsule, adhesins, invasins

71
Q

which 3 mechanisms do the large aiways have to defend against airway infections

A
  1. mucus and coughing
  2. IgA secretion
  3. cilia
72
Q

which 3 mechanisms do small aiways have to defend against airway infections

A
  1. dendritic cells (produce AMPs)
  2. epithelial cells (produce cytokines)
  3. presence of lymphocytes and macrophages
73
Q

how do the alveoli defend against infections

A

type 2 cells which produce type 1 cells

74
Q

what kind of bacterium is Bordatella pertussis and what does it cause

A
  • gram neg coccoide rod

- lower airway infection; whooping cough (kinkhoest)

75
Q

what specific toxin does Bortadella pertussis secrete to kill host epithelial cells

A

adenylate cyclase toxin; increases host cell cAMP

76
Q

what is the role for the S1 subunit in pertussis toxins

A

ADP-ribosylating (adding ADP to target molecules)

77
Q

explain in 6 steps how diphteria toxins works

A
  1. contains A and B part
  2. B attaches to cell
  3. toxin cleaved by protease
  4. A contains ribosylating enzyme and binds NAD
  5. it couples NAD to EF-2 (ADP ribosylated EF-2)
  6. protein synthesis is ceased
78
Q

what is S. pneumoniae for bacterium and what does it cause

A
  • gram pos diplococcus

- abnormal liquid levels in alveoli; inflammation

79
Q

what is special about m. tuberculosis?

A

it is not gram pos or neg, it is Ziehl-Neelsen stained (required for mycobacteria)

Medische Microbiologie (3 decks)

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